Deficient reinforcement learning in medial frontal cortex as a model of dopamine-related motivational deficits in ADHD |
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Affiliation: | 1. Department of Experimental Psychology, Ghent University, Henri Dunantlaan 2, 9000 Ghent, Belgium;2. GIfMI (Ghent Institute for Functional and Metabolic Imaging), Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium;3. Department of Experimental Clinical and Health Psychology, Ghent University, Henri Dunantlaan 2, 9000 Ghent, Belgium;4. Department of Psychology, Shackleton Building (B44), University of Southampton, Highfield Campus, Southampton SO17 1BJ, UK;1. Pediatric Neurology Unit, Quiron University Hospital, Madrid, Spain;2. Department of Biological and Health Psychology, Faculty of Psychology, Autonomous University of Madrid, Madrid, Spain;3. Service, Neuro-Radiology Unit, Magnetic Resonance Unit, Quiron University Hospital, Madrid, Spain;4. Pediatrician, Pediatric Primary Care, Doctor Cirajas Healthcare Center, Madrid, Spain;5. Child-Adolescent Psychiatry Unit, Gómez Ulla Hospital, Madrid, Centro CADE, Madrid, Spain;6. Pediatric Neurology Section, Infanta Leonor Hospital of Vallecas, Madrid, Spain;1. Laboratoire de Neurosciences Cognitives, Institut National de la Santé et de la Recherche Médicale, Paris, France;2. Institut d’Étude de la Cognition, Departement d’Études Cognitives, École Normale Supérieure, Paris, France;1. Department of Psychiatry, Stony Brook University, Stony Brook, NY 11794-8790, United States;2. Department of Pharmacology, Center in Pharmacogenomics, Ohio State University Wexner Medical Center, 333 West 10th Avenue, Columbus 43210, United States |
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Abstract: | Attention Deficit/Hyperactivity Disorder (ADHD) is a pathophysiologically complex and heterogeneous condition with both cognitive and motivational components. We propose a novel computational hypothesis of motivational deficits in ADHD, drawing together recent evidence on the role of anterior cingulate cortex (ACC) and associated mesolimbic dopamine circuits in both reinforcement learning and ADHD. Based on findings of dopamine dysregulation and ACC involvement in ADHD we simulated a lesion in a previously validated computational model of ACC (Reward Value and Prediction Model, RVPM). We explored the effects of the lesion on the processing of reinforcement signals. We tested specific behavioral predictions about the profile of reinforcement-related deficits in ADHD in three experimental contexts; probability tracking task, partial and continuous reward schedules, and immediate versus delayed rewards. In addition, predictions were made at the neurophysiological level. Behavioral and neurophysiological predictions from the RVPM-based lesion-model of motivational dysfunction in ADHD were confirmed by data from previously published studies. RVPM represents a promising model of ADHD reinforcement learning suggesting that ACC dysregulation might play a role in the pathogenesis of motivational deficits in ADHD. However, more behavioral and neurophysiological studies are required to test core predictions of the model. In addition, the interaction with different brain networks underpinning other aspects of ADHD neuropathology (i.e., executive function) needs to be better understood. |
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Keywords: | ADHD ACC Reinforcement learning Dopamine Prediction error Reward expectation |
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